Typical migraine, comprised of migraine with aura (MA) and migraine without aura (MO), is a chronic, painful and debilitating neurovascular disease which is generally characterised by recurrent attacks of severe headache usually accompanied by nausea, vomiting, photo and phonophobia. Migraine has been shown to affect a large proportion of Caucasian populations with a recent comprehensive study indicating that around 25% of women and 8% of men suffer from the disease. Strong familial aggregation of typical migraine and an increased concordance for the disease in MZ twins over DZ twins, suggests that it has a significant genetic component. Heritability estimates are calculated to be between 40% and 60%, indicating that disease variation, in part, is explained by environmental determinants. The mode of transmission of typical migraine is not clear but is most likely multifactorial. Although the MA and MO subtypes exhibit some clinical heterogeneity, segregation analysis has suggested that there may be a common genetic aetiology for MA and MO, and a major gene contributing to typical migraine pathogenesis. This idea is substantiated by the fact that both subtypes of migraine can occur within the same family and even within the same individual, with up to 33% of sufferers experiencing both types of the disease. In addition, migraine prophylactics have been shown to result in similar effects in patients treated for both types of migraine. However, whether the two subtypes are truly separate entities or not remains unclear. At present, the type and number of genes involved in typical migraine is not known. Despite this, several studies into Familial Hemiplegic Migraine (FHM), a very severe subtype of MA, have led to the discovery that mutations in a brain specific calcium channel subunit gene (CACNA1A) located on chromosome 19, cause FHM in about 50% of affected families. FHM is a rare disease and is distinguished from typical migraine by its association with hemiparesis and clear autosomal dominant mode of inheritance. However, certain clinical features are common to both FHM and typical migraine including similarities in headache characteristics and triggers. Hence, FHM genetic studies provide a valuable model for investigating the genes involved in the more prevalent types of migraine with and without aura. For this reason the Genomics Research Centre has been conducting linkage studies utilising large Australian migraine pedigrees with a focus on the known FHM (CACNA1A) gene region on chromosome 19p13. Our results to date have indicated suggestive linkage to the FHM region on 19p13 in a large multigenerational pedigree (MF1) affected with typical migraine, with a maximum parametric LOD score of 1.92 (P = 0.001) obtained for a triplet repeat polymorphism situated in exon 47 of the CACNA1A gene. Expansion of this repeat was not observed, but is possible that mutations elsewhere in the CACNA1A gene may be responsible for migraine in this pedigree. To investigate this possibility, the current research involved sequencing two patients carrying the critical susceptibility haplotype surrounding the CACNA1A gene. The results of this mutation screen revealed no disease causing mutations or polymorphisms in any of the 47 exons screened. To determine whether the CACNA1A genomic region was implicated in typical migraine susceptibility in the general Caucasian population, 82 independent pedigrees and a large case-control group were also analysed using highly polymorphic microsatellite markers. There was no linkage or association detected in these groups and thus, it was concluded that if CACNA1A plays a role in typical migraine it does not confer a major effect on the disease. However, subsequent case-control studies of SNPs in the INSR gene, which is located ~15cM telomeric from CACNA1A, provided evidence of association to typical migraine. Thus, the INSR gene may now emerge as the new migraine susceptibility gene in this genomic region on chromosome 19. Family linkage studies conducted by Gardner et al have implicated an additional FHM susceptibility region on chromsome 1q31. Furthermore, independent research carried out by Ducros et al. has indicated a second FHM locus at 1q21-23, which is ~ 30cM centromeric to the region reported by Gardner et al. At this stage it is not clear whether there is a single locus, or two distinct loci, on the chromosome 1q region. This research also involved a family-based linkage and association approach to investigating the FHM susceptibility region on chromosome 1q31 for involvement in typical migraine susceptibility in affected Australian pedigrees. Initial multipoint ALLEGRO analysis provided strong evidence for linkage of Chr1q31 markers to typical migraine in a large multigenerational pedigree. The 1-LOD* unit support interval for suggestive linkage spanned ~18cM with a maximum allele sharing LOD* score of 3.36 obtained for marker D1S2782, P = 0.00004. Subsequent analysis of an independent sample of 82 affected pedigrees added support to the initial findings with a maximum LOD* of 1.24 (P = 0.008). Utilising the independent sample of 82 pedigrees we also performed a family-based association test. Results of this analysis indicated distortion of allele transmission at marker D1S249 (global c2(5) of 15.00, P = 0.010) in these pedigrees. These positive linkage and association results will need further confirmation by independent researchers, but overall they provide good evidence for the existence of a typical migraine locus near these markers on Chr1q31, and reinforce the idea that an FHM gene in this genomic region may also contribute to susceptibility to the more common forms of migraine. The serotonergic system has long been implicated in the pathophysiology of migraine. Researchers have therefore focused on the serotonin receptors and the genes that code for them when investigating this disease. Although serotonin receptor agonists have proven to be effective in the treatment of migraine, there has been little evidence of a serotonin receptor gene being associated with the disorder. However, in 1998, Ogilvie et al reported that a VNTR in the serotonin transporter gene (SERT) showed altered allelic distributions in a Danish migraine population. In addition to serotonin, there has been renewed interest in the involvement of the dopaminergic pathways in migraine. This interest has gained impetus since the study of Peroutka et al who reported an allelic association between the dopamine receptor gene DRD2 and migraine with aura. Another dopamine related gene, the dopamine beta-hydroxylase gene (DBH), has been localised to Chr 9q34 and codes for the enzyme that catalyses the conversion of dopamine to norepinephrine. It therefore plays an important role in dopaminergic and noradrenergic neurotransmission. Serum levels of DbH enzyme have been reported to be elevated in migrainous patients during the headache phase of an attack. Also, significantly increased DbH enzyme activity has been observed in migraine patients during the headache-free interval. Thus, the DBH gene is another good candidate for involvement in migraine pathophysiology and, to our knowledge, has not been previously implicated in this disease. Candidate gene studies may be useful strategies for identifying genes involved in complex diseases such as migraine, especially if the gene being examined contributes only a minor effect to the overall phenotype. This research also involved a linkage and association approach to investigating neurotransmitter related migraine candidate genes. Specifically, polymorphisms within the serotonin transporter gene (SERT), the dopamine receptor gene (DRD2) and the dopamine beta-hydroxylase (DBH) gene were tested in unrelated Caucasian migraineurs and non-migraine control individuals. In addition, an independent sample of 82 families affected with migraine were examined. Unrelated case-control association analysis of a DBH intragenic dinucleotide polymorphism indicated altered allelic distribution between migraine and control groups (c2 = 16.53, P = 0.019). Furthermore, the transmission/disequilibrium test (TDT) which was implemented on the family data also indicated distortion of allele transmission for the same DBH marker (c2 = 4.44, P = 0.035). Together, these results provide evidence for allelic association of the DBH gene with typical migraine susceptibility (Fisher's Combined P-value = 0.006) and indicate that further research into the role of the DBH gene in migraine aetiology is warranted. Nitric oxide (NO) is emerging as a key molecule affecting the pain associated with migraine. Since nitric oxide synthase (NOS) enzymes catalyse the synthesis of NO, the genes that code for these enzymes are good candidates for migraine molecular genetic analysis. This research involved investigating the role of a functionally relevant bi-allelic tetranucleotide polymorphism located in the promoter region of the human inducible nitric oxide synthase (iNOS) gene in migraine aetiology. A large group of migraine affected individuals were genotyped and compared to an age and sex matched group of unaffected controls. Results of a chi-squared analysis indicated that allele distributions for both migraine cases and controls were not significantly different (c2 = 1.93, P = 0.16). These findings offer no evidence for an allelic association of the tested iNOS polymorphism with the common forms of the disease and therefore do not support a role for this gene in migraine pathogenesis. In summary, this research involved linkage and association analysis of migraine candidate genes and genomic susceptibility regions. Whilst, the known FHM gene (CACNA1A) was excluded for significant involvement in typical migraine the adjacent INSR gene has been associated. Migraine is genetically heterogeneous and the results of this research also provide good evidence that the DBH gene is involved in disease predisposition, whilst the DRD2, SERT and INOS gene were not shown to be implicated. An additional susceptibility region for typical migraine is also likely to localise to chromosome 1q31. Overall, the results presented in this thesis have contributed valuable data to the understanding of the molecular genetics of migraine with and without aura. Future research into the molecular pathophysiological mechanisms of migraine will greatly facilitate the development of more effective diagnosis and treatment strategies.

Copies of author's previously published articles inserted. / Bibliography: leaves 187-209. / xiii, 209 leaves : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Documents the establishment of a reproducible model of carcinoma implanted into the abdominal wall of an immunocompetent Dark agouli rat to study the relationship between laparoscopy and the development of port site metastases. / Thesis (M.D.)--University of Adelaide, Dept. of Surgery, 1998?

Rhodococcus equi is a common cause of severe pneumonia in foals, and is an opportunistic pathogen in immunocompromised humans. In combination, erythromycin and rifampin are the most commonly used antimicrobials in treating R. equi in foals. To provide reliable treatment, it is imperative to determine the mean inhibitory concentrations (MICs) of other antimicrobial agents in the event that certain strains of R. equi develop resistance to the current treatment. Several strains of R. equi have developed resistance to various antibiotics. In this study, R. equi strain 288 was completely resistant to rifampin with a MIC > 256ug/ml. The MICs of ethambutol, clarithromycin, azithromycin, isoniazide, ethionamide, rifampin, erythromycin, and linezolid of ninety-five R. equi isolates were also determined in this study. These isolates were obtained from the lungs and transtracheal washes of foals. In addition to these strains, three National Committee for Laboratory Clinical Standards (NCCLS) quality control strains were also tested: R. equi ATCC 6939, R. equi ATCC 33701, and S. pneumoniae 49619. Each drug was tested in triplicate and the MIC 50’s and MIC 90’s were determined for each drug. Ethambutol, isoniazide, and ethionamide were completely ineffective against R. equi. with MICs > 250ug/ml. Rhodococcus equi strains were more susceptible to clarithromycin (MIC 90 = 0.23 ug/ml) than to azithromycin (MIC 90 = 2.33 ug/ml), rifampicin (MIC 90 = 0.67ug/ml), erythromycin (MIC 90 = 1.2ug/ml), and linezolid (MIC 90 = 4ug/ml).

Cette étude est dédiée à la période charnière que constituent lEifélien et la base du Givétien en Belgique et les régions limitrophes, entre le Dévonien inférieur caractérisé par des dépôts détritiques et linstallation dune plate-forme carbonatée au Givétien. Létude sédimentologique détaillée que nous avons entreprise est le résultat de lintégration de différentes techniques danalyses : sur le terrain (levé et description banc par banc), en lame mince (pétrographie et microfaciès) et sur les échantillons (susceptibilité magnétique et analyses chimiques). Dans le cadre de ce travail, ce sont 14 coupes qui ont été levées, représentant une épaisseur totale de 1650 mètres. Les études de terrain ont permis de mettre en évidence une grande variété de faciès carbonatés, détritiques ou mixtes. Cette variété illustre parfaitement la variabilité latérale qui est la règle au sein de ces niveaux. Les analyses pétrographiques qui ont été menées sur 3352 lames minces, confirment cette diversité et aboutissent à la définition de 71 microfaciès. Ces microfaciès sont répartis sur un modèle de plate-forme et sur 6 modèles de rampe. Ces différents modèles de rampe se distinguent les uns des autres par une influence terrigène plus ou moins marquée, le développement ou non de bioconstructions ou encore la présence ou non de shoals. Les analyses de susceptibilité magnétique on permis de mettre en évidence trois paramètres sédimentologiques principaux linfluençant : lapport détritique (le continent étant la source principale des minéraux porteurs du signal), lagitation (qui peut empêcher le dépôt de ces mêmes minéraux) et la productivité carbonatée (qui peut diluer ces minéraux). Les analyses chimiques quant à elles permettent de clairement dégager 4 pôles parmi les minéraux présents dans les échantillons, chacun ayant sa contribution propre à la valeur de susceptibilité magnétique. Le premier est le contenu en carbonates qui est directement lié à la productivité carbonatée. Outre le quartz détritique, lapport terrigène comporte de son côté deux pôles distincts : lun sous forme dargiles et lautre sous forme de minéraux ferromagnétiques primaires. Le dernier pôle correspond à linfluence de la diagenèse par la dolomitisation et la cristallisation de pyrite, dhématite et éventuellement de magnétite. De par la répartition générale des trois paramètres sédimentologiques cités ci-dessus sur les profils de plate-forme et de rampes, trois types dévolution des courbes de susceptibilité magnétique se dessinent quand on la compare à lévolution des microfaciès. Certaines coupes ne montrent aucun lien entre les deux types de courbes, la susceptibilité magnétique restant relativement constante. Ensuite, un parallélisme peut sobserver entre les deux types de courbes (à une baisse de niveau marin, correspond une hausse de valeurs de susceptibilité magnétique et inversement). Enfin, une opposition peut être observée entre les deux types de courbes (à une baisse de niveau marin, correspond une baisse de valeurs de susceptibilité magnétique et inversement). Une fois identifiés, ces comportements relativement cohérents permettent lutilisation de la susceptibilité magnétique à des fins de corrélation. Lintégration de lensemble des données et interprétations aboutit à la proposition dun canevas de stratigraphie séquentielle. La généralisation de ce canevas à lensemble du bord Sud du Synclinorium de Dinant permet une meilleure compréhension du passage latéral entre la Formation de Couvin et la Formation de Jemelle et de linstallation de la plate-forme carbonatée à la transition Eifélien-Givétien.

Empirically-based models of landslide distribution and susceptibility are currently the most commonly used approach for mapping probabilities of landslide initiation and analyzing their association with natural and anthropogenic environmental factors. In general, these models statistically estimate susceptibility based on the predisposition of an area to experience a landslide given a range of environmental factors, which may include land use, topography, hydrology and other spatial attributes. Novel statistical approaches include the generalized additive model (GAM), a non-parametric regression technique, which is used in this study to explore the relationship of landslide initiation to topography, rainfall and forest land cover and logging roads on Vancouver Island, British Columbia. The analysis is centered on an inventory of 639 landslides of winter 2006/07. Data sources representing potentially relevant environmental conditions of landslide initiation are based on: terrain analysis derived from a 20-m CDED digital elevation model; forest land cover classified from Landsat TM scenes for the summer before the 2006 rainy season; geostatistically interpolated antecedent rainfall patterns representing different temporal scales of rainfall (a major storm, winter and annual rainfall); and the main lithological units of surface geology. In order to assess the incremental effect of these data sources to predict landslide susceptibility, predictive performances of models based on GAMs are compared using spatial cross-validation estimates of the area under the ROC curve (AUROC), and variable selection frequencies are used to determine the prevalence of non-parametric associations to landslides. In addition to topographic variables, forest land cover (e.g., deforestation), and logging roads showed a strong association with landslide initiation, followed by rainfall patterns and the very general lithological classification as less important controls of landscape-scale landslide activity in this area. Annual rainfall patterns are found not to contribute significantly to model prediction improvement and may lead to model overfitting. Comparisons to generalized linear models (i.e., logistic regression) indicate that GAMs are significantly better for modeling landslide susceptibility. Overall, based on the model predictions, the most susceptible 4% of the study area had 29 times higher density of landslide initiation points than the least susceptible 73% of the study area (0.156 versus 0.005 landslides/km2).

Deregulation of autophagy plays an important role in the pathogenesis of diseases such as cancer, neuronal degenerative or cardiovascular disease. Autophagy is a process to engulf the cytoplasmic contents into autophagosome and deliver them for lysosomal degradation. Its major function is to clear unfolded protein or damage organelles for maintaining proper metabolic homeostasis and normal cell physiological activities. Autophagy and multivesicular bodies, MVBs, cooperate to regulate the turnover of intracellular macromolecule, defective organelles and signaling receptor. Endosomal sorting complex required for transport, ESCRT, is important for the formation of MVBs, which regulates membrane receptor recycling, protein sorting and vesicular trafficking. Tumor Susceptibility Gene 101(TSG101) is a member of ESCRT-I that plays an important role on MVBs formation and maintaining ESCRT function. Previous report indicated that autophagosome accumulation upon deprivation of TSG101, implying possible role of TSG101 during autophagic process. In this study, we observed the increase of TSG101 and autophagic marker proteins, such as LC3-II and ATG upon nutrient starvation. Furthermore, knockdown TSG101 in cervical carcinoma HeLa cell resulted in the elevation of LC3-II, ATG3 and ubiquitinated protein aggregates marker protein p62, which is congruous to other reports. However, in neuroblastoma SH-SY5Y cell, transfection of siRNA led to the decrease of LC-II and ubiquitinated protein level. These results indicated that TSG101 might be critical for autophagy and the maintenance of steady-state level of cellular ubiquitinated proteins. Ectopic upregulatory expression of HA-TSG101 led to the increase of LC3-II in both cell type. The elevation of ATG3 level is also observed in HeLa cell. Therefore, we speculated that TSG101 might be important for the formation of autophagosome, but our data did not exclude the possible role of TSG101 in regulation of the fusion of autophagosome and lysosome, because the increase of ATG3 indicated ectopic HA-TSG101 might facilitate the execution of autophagic flow. In addition, we have established GFP-LC3 expression cell lines. Our imaging data showed the colocalization of TSG101 and GFP-LC3 in both cytoplasm and nucleus that might be an interesting research topic for investigation the role of TSG101 in autophagic pathway.

Rhodococcus equi is a common cause of severe pneumonia in foals, and is an opportunistic pathogen in immunocompromised humans. In combination, erythromycin and rifampin are the most commonly used antimicrobials in treating R. equi in foals. To provide reliable treatment, it is imperative to determine the mean inhibitory concentrations (MICs) of other antimicrobial agents in the event that certain strains of R. equi develop resistance to the current treatment. Several strains of R. equi have developed resistance to various antibiotics. In this study, R. equi strain 288 was completely resistant to rifampin with a MIC > 256ug/ml. The MICs of ethambutol, clarithromycin, azithromycin, isoniazide, ethionamide, rifampin, erythromycin, and linezolid of ninety-five R. equi isolates were also determined in this study. These isolates were obtained from the lungs and transtracheal washes of foals. In addition to these strains, three National Committee for Laboratory Clinical Standards (NCCLS) quality control strains were also tested: R. equi ATCC 6939, R. equi ATCC 33701, and S. pneumoniae 49619. Each drug was tested in triplicate and the MIC 50’s and MIC 90’s were determined for each drug. Ethambutol, isoniazide, and ethionamide were completely ineffective against R. equi. with MICs > 250ug/ml. Rhodococcus equi strains were more susceptible to clarithromycin (MIC 90 = 0.23 ug/ml) than to azithromycin (MIC 90 = 2.33 ug/ml), rifampicin (MIC 90 = 0.67ug/ml), erythromycin (MIC 90 = 1.2ug/ml), and linezolid (MIC 90 = 4ug/ml).

Studying hurricane preparedness among the Resident Assistants (RAs) and Residence Life Coordinators (RLCs) at Louisiana State University (LSU) is imperative to assure that the university housing staff is fully equipped when faced with an oncoming threat. This study seeks to fill a gap in research by investigating the influences of preparedness on student housing employees. A survey was developed and the measures were found to be coherent and internally reliable through the use of factor analysis. Based on theory and previous literature, a linear regression model was developed that quantified the relationship between the independent variable of preparedness and general knowledge, past experience, preparation anxiety, threat anxiety, amount of time as a housing employee, amount of time living in Baton Rouge, location of primary address, gender, ethnicity, and car access. Only general knowledge and preparation anxiety were found to influence the preparedness construct significantly (at the 5 percent level). Demographic factors did not influence hurricane preparedness levels of housing staff employees. Results suggest that the university acts as a buffer to student populations from typical vulnerabilities that the regular population experiences in disaster scenarios. This research could be applicable to other university housing staff employees who work at a university that may be frequently impacted by hurricanes.

Nearly every species on the planet has at least one parasite, which, by definition, incurs a cost in the host. Therefore, organisms must resist parasites - preventing or reducing infections - or tolerate parasites - reducing the costs of infection - in order to maintain their fitness despite the presence of parasites. Here, I investigated: 1) whether parasitic, larval trematodes (cercariae) can detect the least resistant tadpole host species, 2) a hypothetical framework for how host life history impacts the utilization of inflammation and thus, resistance and tolerance, 3) whether a common anesthesia technique used in experimental infections immunocompromises tadpoles, 4) the relationship between tadpole host life history, tolerance, and behavioral resistance to cercarial infection, 5) how tadpole behavior affects trematode infection location, and 6) how host life history impacts trematode infection location and the implications of this for host tolerance. In the first chapter, I investigated whether trematode cercariae could discriminate among several tadpole host species to identify the most susceptible hosts. Cercariae were consistently more attracted to Bufo terrestris tadpoles, which was the most susceptible host species. Other tadpole species varied in attractiveness in an order similar to their susceptibility to infection. Furthermore, there was consistent and significant variation among individual attractiveness and susceptibility within host species. If susceptibility to infection is heritable, chemical cues used by cercariae to identify susceptible hosts could represent a substrate on which natural selection acts, setting up a "Red Queen" arms race between host cues and parasite detection of those cues. In the second chapter, I proposed a framework which outlined the cost-benefit relationship between host life history and immune responses. Because inflammatory immune responses are known to cause self-damage to hosts, anti-inflammatory immune responses should vi be used for long-lived, slowly-developing ("slow-paced") hosts, those infected with relatively less virulent parasites, and/or ongoing but ineffective inflammatory responses. Conversely, the cost of inflammation might be less expensive than the cost of infection among shortlived, rapidly-developing ("fast-paced") hosts, those infected with virulent parasites, and/or those undergoing protracted but ineffective anti-inflammatory immune responses. In the third research chapter, I investigated whether two common anesthesia agents, benzocaine and tricaine mesylate (MS-222), immunocompromise tadpoles. These chemicals are used extensively to study the behavioral resistance of tadpoles to cercariae; if treatment increases infections not only by removing these behaviors but also by suppressing the immune system, behavior might appear artificially effective at preventing trematode infection. I found that neither benzocaine nor MS-222 affected the abundance of circulating white blood cells relative to waterexposed control tadpoles. Furthermore, there was no difference in trematode infection success when tadpoles were anesthetized, allowed to recover from anesthesia, and subsequently experimentally infected. The results of this experiment indicate that benzocaine and MS-222 are both practical, non-immunosuppressive anesthesia agents to use when studying trematode infections in amphibians. In the fourth research chapter, I quantified tadpole hosts' use of behavioral resistance (parasite-induced behaviors) and tolerance of exposure to cercariae. Across seven host species, parasite-induced behaviors were negatively correlated with pace-of-life, with rapidly-developing ("fast-paced") tadpoles exhibiting significantly more behavior than slowly-developing ("slowpaced") tadpoles. The opposite pattern was true of tolerance, where fast-paced species had poorer tolerance of cercarial exposure than slow-paced species. Given that slow-paced species are more likely to be exposed to cercariae because they 1) occur in water more likely to harbor cercariae and 2) have longer developmental times, tolerance to trematode exposure might be an vii evolutionary adaptation that circumvents the costs of behavioral - and, possibly, immunological - resistance to infection. In the fifth research chapter, I investigated whether parasite-induced behaviors were capable of affecting encystment location of trematode cercariae in Hyla femoralis tadpoles and whether the resulting encystment location affected tolerance of infection. Benzocaineanesthetized and control tadpoles had similar infection intensities. However, among benzocaineanesthetized tadpoles, the majority of cercarial infections occurred in tadpoles' heads, but unanesthetized control tadpoles were predominantly tail-infected. Furthermore, the number of head infections were negatively associated with mass change (poor tolerance), whereas the number of tail infections was positively associated with mass change (good tolerance). These results suggest that parasite-induced behavior is not only an important mechanism of resistance to trematodes, as other researchers have described, but also a mechanism of tolerance, whereby tadpoles can prevent the deleterious effects of trematode infection by controlling infection location. The sixth research chapter extends the work of the fifth and investigates whether host life history predicts encystment location of cercariae and whether encystment location affects tolerance of infection. Among seven host species, fast-paced species had significantly more infections in the head and body, whereas slow-paced species had the majority of infections in their tails. Slow-paced species were also less resistant to trematode infections in any body location than fast-paced species. These patterns were partially explained by surface area, with a slow-paced species having more surface area (making them more likely to be contacted and infected by cercariae) and a larger proportion of slow-paced species' surface area was comprised by tail than heady and body. Tail infections were less expensive than head and body infections; slow-paced species were more tolerant of infection and across species, tail infections had no effect on tolerance (mass change) whereas head infections were negatively associated with tolerance. These results suggest that slow-paced tadpoles, which are relatively more likely to viii become infected by cercariae and probably have more evolutionary history with these parasites, have invested in a morphology that improves their tolerance to parasites. The body of work that I have produced demonstrates that variation in resistance and tolerance to trematode parasites is ubiquitous among tadpole hosts. Furthermore, this variation is predictable based on host life history. Because tadpole life history can dramatically impact the likelihood of exposure to cercariae and encounters are necessary for host-parasite selective pressure to occur, life history can predict the adaptations of hosts and parasites. Given amphibians' status as the most rapidly declining taxon on the planet and the ubiquity of emerging infectious diseases for amphibians and other organisms, these findings should inform future research on host- and parasite-mediated mechanisms of disease.

The Stone Age settlement site outside the village of Vuollerim in northern Sweden was first discovered in the 1980s and has been an important part of the research regarding Mesolithic and Neolithic in Norrland. One of the houses on the site was named Norpan 2 and nearly fifteen hundred soil samples were collected and stored during the excavations between 1983 and 1987. This study has focused on analysing nearly one thousand of the collected soil samples using phosphate and magnetic susceptibility analysis to further study activity on site and social structure. Furthermore, due to the large quantity of samples, a short comparison of soil sampling density was made to perceive the effect sampling density has on the interpretation of soil mapping. The results of the study indicate that the site has a large deposit of Magnetite (Fe3O4) in the soil that gives unusual MS-readings from the collected samples. The results also show a bipolar separation of finds and geoarchaeological traces within the house. This distinctive separation has been argued as an indication of dividing the space between families, but this study indicate that this separation might be due to house being divided between different activities but the evidence is not conclusive enough without further studies. The study has also shown that while a high density soil mapping gives much greater details it is still possible to gain the necessary information with fewer samples. In conclusion, it is still too early to conclude the investigations at the Vuollerim site and with the added data from this study and new information there is still more to learn from the Vuollerim site.KeywordsPhosphate analysis, Magnetic susceptibility, Vuollerim, Norpan 2, Geoarchaeology, Soil mapping