Low-intensity red and infrared laser effects at high fluences on Escherichia coli cultures

Semiconductor laser devices are readily available and practical radiation sources providing wavelength tenability and high monochromaticity. Low-intensity red and near-infrared lasers are considered safe for use in clinical applications. However, adverse effects can occur via free radical generation, and the biological effects of these lasers from unusually high fluences or high doses have not yet been evaluated. Here, we evaluated the survival, filamentation induction and morphology of Escherichia coli cells deficient in repair of oxidative DNA lesions when exposed to low-intensity red and infrared lasers at unusually high fluences. Cultures of wild-type (AB1157), endonuclease III-deficient (JW1625-1), and endonuclease IV-deficient (JW2146-1) E. coli, in exponential and stationary growth phases, were exposed to red and infrared lasers (0, 250, 500, and 1000 J/cm2) to evaluate their survival rates, filamentation phenotype induction and cell morphologies. The results showed that low-intensity red and infrared lasers at high fluences are lethal, induce a filamentation phenotype, and alter the morphology of the E. coli cells. Low-intensity red and infrared lasers have potential to induce adverse effects on cells, whether used at unusually high fluences, or at high doses. Hence, there is a need to reinforce the importance of accurate dosimetry in therapeutic protocols.

Effects of Obesity and Weight Loss Following Bariatric Surgery on Brain Function, Structural Integrity and Metabolism

Obesity is one of the key challenges to health care system worldwide and its prevalence is estimated to rise to pandemic proportions. Numerous adverse health effects follow with increasing body weight, including increased risk of hypertension, diabetes, hypercholesterolemia, musculoskeletal pain and cancer. Current evidence suggests that obesity is associated with altered cerebral reward circuit functioning and decreased inhibitory control over appetitive food cues. Furthermore, obesity causes adverse shifts in metabolism and loss of structural integrity within the brain. Prior cross-sectional studies do not allow delineating which of these cerebral changes are recoverable after weight loss. We compared morbidly obese subjects with healthy controls to unravel brain changes associated with obesity. Bariatric surgery was used as an intervention to study which cerebral changes are recoverable after weight loss. In Study I we employed functional magnetic resonance imaging (fMRI) to detect the brain basis of volitional appetite control and its alterations in obesity. In Studies II-III we used diffusion tensor imaging (DTI) and voxel-based morphometry (VBM) to quantify the effects of obesity and the effects of weight loss on structural integrity of the brain. In study IV we used positron emission tomography (PET) with [18F]-FDG in fasting state and during euglycemic hyperinsulinemia to quantify effects of obesity and weight loss on brain glucose uptake. The fMRI experiment revealed that a fronto-parietal network is involved in volitional appetite control. Obese subjects had lower medial frontal and dorsal striatal brain activity during cognitive appetite control and increased functional connectivity within the appetite control circuit. Obese subjects had initially lower grey matter and white matter densities than healthy controls in VBM analysis and loss of integrity in white matter tracts as measured by DTI. They also had initially elevated glucose metabolism under insulin stimulation but not in fasting state. After the weight loss following bariatric surgery, obese individuals’ brain volumes recovered and the insulin-induced increase in glucose metabolism was attenuated. In conclusion, obesity is associated with altered brain function, coupled with loss of structural integrity and elevated glucose metabolism, which are likely signs of adverse health effects to the brain. These changes are reversed by weight loss after bariatric surgery, implicating that weight loss has a causal role on these adverse cerebral changes. Altogether these findings suggest that weight loss also promotes brain health.Key words: brain, obesity, bariatric surgery, appetite control, structural magnetic resonance

Prions: the danger of biochemical weapons

The knowledge of biotechnology increases the risk of using biochemical weapons for mass destruction. Prions are unprecedented infectious pathogens that cause a group of fatal neurodegenerative diseases by a novel mechanism. They are transmissible particles that are devoid of nucleic acid. Due to their singular characteristics, Prions emerge as potential danger since they can be used in the development of such weapons. Prions cause fatal infectious diseases, and to date there is no therapeutic or prophylactic approach against these diseases. Furthermore, Prions are resistant to food-preparation treatments such as high heat and can find their way from the digestive system into the nervous system; recombinant Prions are infectious either bound to soil particles or in aerosols. Therefore, lethal Prions can be developed by malicious researchers who could use it to attack political enemies since such weapons cause diseases that could be above suspicion.

Ultrastructural changes of Fusobacterium nucleatum as a defense mechanism against human neutrophil peptide-1 - A Transmission Electron Microscopy (TEM) study

Aims: The aim of this work was to assess the ultrastructural changes, cellular proliferation, and the biofilm formation ability of F. nucleatum as defense mechanisms against the effect of HNP-1. Materials and methods: The type strain of F. nucleatum (ssp. nucleatum ATCC 25586) and two clinical strains (ssp. polymorphum AHN 9910 and ssp. nucleatum AHN 9508) were cultured and incubated with four different test concentrations of recombinant HNP-1 (1, 5, 10 and 20 µg/ml) and one control group (0 µg/ml). Bacterial pellets from each concentration were processed for TEM imaging. Planktonic growth was assessed and colony forming units (CFU) were measured to determine the cellular proliferation. Scrambled HNP-1 was used for confirmation. Results: TEM analyses revealed a decrease in the outer membrane surface corrugations and roughness of the strain AHN 9508 with increasing HNP-1 concentrations. In higher concentrations of HNP-1, the strain AHN 9910 showed thicker outer membranes with a number of associated rough vesicles attached to the outer surface. For ATCC 25586, the treated bacterial cells contained higher numbers of intracellular granules with increasing the peptide concentration. Planktonic growth of the two clinical strains were significantly enhanced (P<0.001) with gradually increased concentrations of HNP-1. None of the planktonic growth results of the 3 strains incubated with the scrambled HNP-1 was statistically significant. HNP-1 decreased the biofilm formation of the two clinical strains, AHN 9910 and 9508, significantly (P<0.01 and P<0.001; respectively). Conclusions: The present in vitro study demonstrates that F. nucleatum has the ability to withstand the lethal effects of HNP-1 even at concentrations simulating the diseased periodontium in vivo. The increase in planktonic growth could act as defense mechanisms of F. nucleatum against HNP-1.

“Who is steering the ship and which constellation guides the way? Exploring transparency in the European Central Bank during the time of crisis”

This paper explores transparency in the decision-making of the European Central Bank (ECB). According to ECB´s definition, transparency means that the central bank provides the general public with all relevant information on its strategy, assessments and policy decisions as well as its procedures in an open, clear and timely manner. In this paper, however, the interpretation of transparency is somewhat broader: Information is freely available and directly accessible to those who will be affected by the decisions. Moreover, the individuals shall be able to master this material. ECB´s negative attitude towards publication of documents has demonstrated central bank´s reluctance to strive towards more extensive transparency. By virtue of the definition adopted by the ECB the bank itself is responsible for determining what is considered as relevant information. On the grounds of EU treaties, this paper assesses ECB`s accountability concentrating especially on transparency by employing principal-agent theory and constitutional approach. Traditionally, the definite mandate and the tenet of central bank independence have been used to justify the limited accountability. The de facto competence of the ECB has, however, considerably expanded as the central bank has decisively resorted to non-standard measures in order to combat the economic turbulences facing Europe. It is alleged that non-standard monetary policy constitutes a grey zone occasionally resembling economic policy or fiscal policy. Notwithstanding, the European Court of Justice has repeatedly approved these measures. This dynamic interpretation of the treaties seems to allow temporarily exceptions from the central bank´s primary objective during extraordinary times. Regardless, the paper suggests that the accountability nexus defined in the treaties is not sufficient in order to guarantee the accountability of the ECB after the adoption of the new, more active role. Enhanced transparency would help the ECB to maintain its credibility. Investing in the quality of monetary dialogue between the Parliament and the ECB appears to constitute the most adequate and practicable method to accomplish this intention. As a result of upgraded transparency the legitimacy of the central bank would not solely rest on its policy outputs.

Characterisation of Cladonia rangiferina transcriptome and genome, and the effects of dehydration and rehydration on its gene expression

Lichens are symbiotic organisms, which consist of the fungal partner and the photosynthetic partner, which can be either an alga or a cyanobacterium. In some lichen species the symbiosis is tripartite, where the relationship includes both an alga and a cyanobacterium alongside the primary symbiont, fungus. The lichen symbiosis is an evolutionarily old adaptation to life on land and many extant fungal species have evolved from lichenised ancestors. Lichens inhabit a wide range of habitats and are capable of living in harsh environments and on nutrient poor substrates, such as bare rocks, often enduring frequent cycles of drying and wetting. Most lichen species are desiccation tolerant, and they can survive long periods of dehydration, but can rapidly resume photosynthesis upon rehydration. The molecular mechanisms behind lichen desiccation tolerance are still largely uncharacterised and little information is available for any lichen species at the genomic or transcriptomic level. The emergence of the high-throughput next generation sequencing (NGS) technologies and the subsequent decrease in the cost of sequencing new genomes and transcriptomes has enabled non-model organism research on the whole genome level. In this doctoral work the transcriptome and genome of the grey reindeer lichen, Cladonia rangiferina, were sequenced, de novo assembled and characterised using NGS and traditional expressed sequence tag (EST) technologies. RNA extraction methods were optimised to improve the yield and quality of RNA extracted from lichen tissue. The effects of rehydration and desiccation on C. rangiferina gene expression on whole transcriptome level were studied and the most differentially expressed genes were identified. The secondary metabolites present in C. rangiferina decreased the quality – integrity, optical characteristics and utility for sensitive molecular biological applications – of the extracted RNA requiring an optimised RNA extraction method for isolating sufficient quantities of high-quality RNA from lichen tissue in a time- and cost-efficient manner. The de novo assembly of the transcriptome of C. rangiferina was used to produce a set of contiguous unigene sequences that were used to investigate the biological functions and pathways active in a hydrated lichen thallus. The de novo assembly of the genome yielded an assembly containing mostly genes derived from the fungal partner. The assembly was of sufficient quality, in size similar to other lichen-forming fungal genomes and included most of the core eukaryotic genes. Differences in gene expression were detected in all studied stages of desiccation and rehydration, but the largest changes occurred during the early stages of rehydration. The most differentially expressed genes did not have any annotations, making them potentially lichen-specific genes, but several genes known to participate in environmental stress tolerance in other organisms were also identified as differentially expressed.

Trophic cascades in boreal landscapes: top predator protection on tree seedlings and forest grouse

Changes in the abundance of top predators have brought about notable, cascading effects in ecosystems around the world. In this thesis, I examined several potential trophic cascades in boreal ecosystems, and their separate interspecific interactions. The main aim of the thesis was to investigate whether predators in the boreal forests have direct or indirect cascading effects on the lower trophic levels. First, I compared the browsing effects of different mammalian herbivores by excluding varying combinations of voles, hares and cervids from accessing the seedlings of silver birch (Betula pendula), Scots pine (Pinus sylvestris) and Norway spruce (Picea abies). Additionally, I studied the effect of simulated predation risk on vole browsing by using auditory cues of owls. Moving upwards on the trophic levels, I examined the intraguild interactions between the golden eagle (Aquila chrysaetos), and its mesopredator prey, the red fox (Vulpes vulpes) and the pine marten (Martes martes). To look at an entire potential trophic cascade, I further studied the combined impacts of eagles and mesopredators on the black grouse (Tetrao tetrix) and the hazel grouse (Tetrastes bonasia), predicting that the shared forest grouse prey would benefit from eagle presence. From the tree species studied, birch appears to be the most palatable one for the mammalian herbivores. I observed growth reductions in the presences of cervids and low survival associated with hares and voles, which suggests that they all weaken regeneration in birch stands. Furthermore, the simulated owl predation risk appeared to reduce vole browsing on birches in late summer, although the preferred grass forage is then old and less palatable. Browsing by voles and hares had a negative effect on the condition and survival of Scots pine, but in contrast, the impact of mammalian herbivores on spruce was found to be small, at least when more preferred food is available. I observed that the presence of golden eagles had a negative effect on the abundance of adult black grouse but a positive, protective effect on the proportion of juveniles in both black grouse and hazel grouse. Yet, this positive effect was not dependent on the abundance foxes or martens, nor did eagles seem to effectively decrease the abundance of these mesopredators. Conversely, the protection effect on grouse could arise from fear effects and also be mediated by other mesopredators. The results of this thesis provide important new information about trophic interactions in the boreal food webs. They highlight how different groups of mammalian herbivores vary in their effects on the growth and condition of different tree seedlings. Lowered cervid abundances could improve birch regeneration, which indirectly supports the idea that the key predators of cervids could cause cascading effects also in Fennoscandian forests. Owls seem to reduce vole browsing through an intimidation effect, which is a novel result of the cascading effects of owl vocalisation and could even have applications for protecting birch seedlings. In the third cascade examined in this thesis, I found the golden eagle to have a protective effect on the reproducing forest grouse, but it remains unclear through which smaller predators this effect is mediated. Overall, the results of this thesis further support the idea that there are cascading effects in the forests of Northern Europe, and that they are triggered by both direct and non‐lethal effects of predation.

Identification and validation of novel prostate cancer biomarkers

Prostate cancer (PCa) has emerged as the most commonly diagnosed lethal cancer in European men. PCa is a heterogeneous cancer that in the majority of the cases is slow growing: consequently, these patients would not need any medical treatment. Currently, the measurement of prostate-specific antigen (PSA) from blood by immunoassay followed by digital rectal examination and a pathological examination of prostate tissue biopsies are the most widely used methods in the diagnosis of PCa. These methods suffer from a lack of sensitivity and specificity that may cause either missed cancers or overtreatment as a consequence of over-diagnosis. Therefore, more reliable biomarkers are needed for a better discrimination between indolent and potentially aggressive cancers. The aim of this thesis was the identification and validation of novel biomarkers for PCa. The mRNA expression level of 14 genes including AMACR, AR, PCA3, SPINK1, TMPRSS2-ERG, KLK3, ACSM1, CACNA1D, DLX1, LMNB1, PLA2G7, RHOU, SPON2, and TDRD1 was measured by a truly quantitative reverse transcription PCR in different prostate tissue samples from men with and without PCa. For the last eight genes the function of the genes in PCa progression was studied by a specific siRNA knockdown in PC-3 and VCaP cells. The results from radical prostatectomy and cystoprostatectomy samples showed statistically significant overexpression for all the target genes, except for KLK3 in men with PCa compared with men without PCa. Statistically significant difference was also observed in low versus high Gleason grade tumors (for PLA2G7), PSA relapse versus no relapse (for SPON2), and low versus high TNM stages (for CACNA1D and DLX1). Functional studies and siRNA silencing results revealed a cytotoxicity effect for the knock-down of DLX1, PLA2G7, and RHOU, and altered tumor cell invasion for PLA2G7, RHOU, ACSM1, and CACNA1D knock-down in 3D conditions. In addition, effects on tumor cell motility were observed after silencing PLA2G7 and RHOU in 2D monolayer cultures. Altogether, these findings indicate the possibility of utilizing these new markers as diagnostic and prognostic markers, and they may also represent therapeutic targets for PCa.

Recueil de lettres originales et de copies de pièces indiquées comme telles dans le dépouillement qui suit.

Contient : 1 Lettre de « MAURITIO, card[inal] DE SAVOYE », au duc de Nemours. « Ce 21 janvier 1616 » ; 2 Lettre de « THOMAS FR[ANÇOIS] » DE SAVOIE, prince DE CARIGNAN, au duc de Nemours. « A Thurin, ce 25 de janvier 1616 » ; 3 Lettre de « HENRY DE SAVOYE [duc DE NEMOURS]... à monsieur Dormy, intendant de ma maison... Du XXIIIme mars 1616 » ; 4 Lettre de « don PEDRO DE TOLEDO OSORIO,... al señor duque de Namurs,... De Milan, 15 de mayo 1616 ». En espagnol ; 5 Lettre de « C. FRERE,... à monseigneur le duc de Nemours,... A La Vapilliere, ce 17 may 1616 » ; 6 Lettre du Sr « CARRON,... à monsieur de La Grange,... Ce 14 de juillet 1616 » ; 7 Lettre de « J[EAN] P[IERRE] CAMUS, e[vêque] de Belley,... à monseigneur le duc de Genevois, de Nemour et de Chartres,... 21 juillet 1616 » ; 8 Lettre du Sr « CARRON » au duc de Nemours. « Anecy, ce 25 de julliet 1616 » ; 9 « Letre en forme de manifeste de S. A. [CHARLES EMANUEL, duc DE SAVOIE] à monseigneur d'Alincourt,... De Turin, ce quatriesme aoust 1616 ». Copie ; 10 Lettre de « JUAN DE AYÇAGA,... al duque de Nemurs,... De Biçançon, a 27 de agosto 1616 ». En espagnol ; 11 Lettre de « JUAN DE AYÇAGA » au duc de Nemours. « De Biçançon, 11 de agosto 1616 ». En espagnol ; 12 Lettre de « don PEDRO DE TOLEDO OSORIO,... al illmo señor de Nemurs,... De Milan, 6 de agosto 1616 ». En espagnol ; 13 Lettre de « don PEDRO DE TOLEDO OSORIO,... al illmo señor de Nemurs,... De Pavia, a 15 de agosto 1616 ». En espagnol ; 14 Lettre de « don PEDRO DE TOLEDO OSORIO,... al illmo señor de Nemurs,... De Pavia, a 17 de agosto 1616 ». En espagnol ; 15 Lettre du Sr « BOLOGNE, abbate de Sancto Martino... a madama de Ferrara,... Di Fontanableo, questo XXVIII d'agosto 1616 ». En italien ; 16 Lettre de « HENRY DE SAVOYE [duc DE NEMOURS]... à monsieur Dormy,... De Lagneux, le dernier jour d'aoust 1616 » ; 17 Lettre de « JUAN DE AYÇAGA » au duc de Nemours. « A primo di septembre 1616 ». Copie ; 18 Lettre de « don JUAN VIVAS,... al señor duque de Nemurs,... De Genova, a 6 de julio 1616 ». En espagnol ; 19 Lettre du Sr « VERRUE » au duc de Nemours. « Thurin, ce 13me septembre 1616 » ; 20 « Copie de letre escripte au seignor dom Petro par Mr DE LA GRANGE,... Ce 13e septembre 1616 » ; 21 Lettre de « B. FORAX » au duc de Nemours. « Par???is, ce 19me septembre 1616 » ; 22 Lettre de « M[AURICE], cardinal DE SAVOYE,... à monsieur le duc de Nemours,... De Rome, le 20 septembre 1626 » ; 23 Lettre de « B. FORAX,... à monseigneur le duc de Nemours,... A Paris, ce 24me septembre 1616 » ; 24 Lettre du « marquis DE RYE,... à monseigneur le duc de Nemours,... De Grey, ce 30 de septembre 1616 » ; 25 Lettre de CHARLES DE NEUFVILLE, marquis « D'ALINCOURT,... à monseigneur le duc de Nemours,... De Lion, ce 30e de septembre 1616 » ; 26 Lettre de « MARIE [DE MEDICIS]... à mon cousin le duc de Nemours,... Escrit à Paris, le XIXe jour d'octobre 1616 » ; 27 Lettre de « B. FORAX » au duc de Nemours. « A Paris, ce 10me octobre 1616 » ; 28 Lettre de CHARLES DE « CREQUY [DE CANAPLES]... à monsieur le duc de Nemours,... A Grenoble, le 25 de novembre 1616 » ; 29 Lettre de « B. FORAX » au duc de Nemours. « A Paris, ce 2me decembre 1616 » ; 30 Lettre de CHARLES EMMANUEL, duc DE SAVOIE, au maréchal de Lesdiguières. « De Turin, le 3e decembre 1616 ». Copie ; 31 Lettre de FRANÇOIS DE BONNE, maréchal DE « LESDIGUIERES », au duc de Nemours. « Ce Ve decembre 1616, à Grenoble » ; 32 Lettre de « GIOAN BATTISTA VASSALO » au duc de Nemours. « Di Parigi, li 10 decembre 1616 ». En italien ; 33 Lettre de « MARIE DE BOURBON [SOISSONS, princesse DE CARIGNAN]... à monsieur le duc de Nemours,... A Turin, ce 16 de novembre 1626 » ; 34 Lettre de « MARIE DE BOURBON [SOISSONS, princesse DE CARIGNAN]... à madame la duchesse de Nemours,... De Turin, ce 16 novembre 1626 » ; 35 Lettre des « commissaires generaux au païs de Valley... à messieurs de la chambre des comptes du Genevois... De Sion, ce 17/27 decembre 1616 » ; 36 Lettre de « MARIE [DE MEDICIS]... à mon cousin le duc de Nemours,... De Paris, le XXe decembre 1626 » ; 37 Lettre de JACQUES DE MONTGOMMERY « DE CORBOUZON,... à monseigneur le duc de Nemours,... Ce 17 janvier 1617 » ; 38 Lettre de « B. FORAX » au duc de Nemours. « A Paris, ce 21me janvier 1617 » ; 39 Lettre de JACQUES DE MONTGOMMERY « DE CORBOUZON,... à monseigneur le duc de Nemours,... De Paris, le 22 janvier 1617 » ; 40 Lettre de FRANÇOIS DE BONNE, maréchal DE « LESDIGUIERES », au duc de Nemours. « Ce 26 janvier 1617, à Turin » ; 41 Lettre de JACQUES DE MONTGOMMERY « DE CORBOUZON,... à monseigneur le duc de Nemours,... Ce 10 fevrier 1617 » ; 42 Fragment d'une lettre de femme sollicitant une explication. « C'est de Grenoble, ce 25 juin 1617 » ; 43 Lettre de « C[HARLES] EMANUEL [duc DE SAVOIE]... à mon frere, monsieur le duc de Genevois et de Nemours,... De Thurin, ce 27 decembre 1617 » ; 44 « Commission pour la revision des comptes [de tutelle de Henri d'Orléans, duc de Longueville]... Donné à Paris, le septiesme jour de juin, l'an de grace mil six cens dix sept ». Copie ; 45 « Commission pour la revision des comptes de [tutelle de Henri d'Orléans, duc de Longueville]... Donné à Paris, le dernier jour de juin, l'an de grace M.VI.C.XIII ». Copie ; 46 Brevet du roi, par lequel il est ordonné que « l'abbaye de St Estienne de Caen sera unie et annexée à la mense archiepiscopale de l'archevesché de Rouen... XVIIIe de febvrier, l'an mil six cens dix huit ». Copie ; 47 Requête adressée par « HENRY DE SAVOYE », duc DE NEMOURS, à « S. A. » le duc de Savoie, pour le prier « de voulloir faire la nommination des chevalliers » de l'Annonciade. « A Paris, mil six cens dix huict » ; 48 Lettre de « FRANÇOIS [DE SALES], e[vêque] de Geneve », au duc de Nemours. « XI may 1618, Annessi » ; 49 Lettre du « prince de Piemont V[ITTORE] AMEDEO,... à monsieur de Nemours,... A Turin, le 18 julliet 1618 » ; 50 Lettre de « M[AURICE], cardinal DE SAVOYE,... à madame de Nemours,... De Turin, le 20 juliet 1618 » ; 51 Lettre de « THOMAS » FRANÇOIS DE SAVOIE, prince DE CARIGNAN, au duc de Nemours. « Julliet 1618, à Thurin » ; 52 Lettre de « M[AURICE], cardinal DE SAVOYE,... à madame de Nemours,... Turin, le 14 aoust 1618 » ; 53 Lettre de l'archiduchesse « ISABEL [CLARA EUGENIA]... a la duquesa de Nemurs,... 1618 ». En espagnol ; 54 Lettre de « FRANÇOIS DE LORRAINE [comte DE VAUDEMONT]... à monsieur le duc de Nemours,... A Toul, le XXIII de mars 1619 » ; 55 Lettre de « CLAUDIO MARINI,... al duca de Nemours,... A Torino, 5 di aprile 1619 ». En italien ; 56 Lettre de « FRANCESCO AURELIO BRAIDA,... al duca di Nemours,... Di Torino, alli 8 di aprile 1619 ». En italien ; 57 Lettre de « GERARDO BASSO » au duc de Nemours. « Di Genova, a di 25 giugno 1619 ». En italien ; 58 Lettre de « CHRESTIENNE [DE FRANCE, princesse de Piémont]... à monsieur de Nemours, mon cousin » ; 59 « Lettre de « CHRESTIENNE [DE FRANCE, princesse de Piémont]... à madame de Nemours,... De Turin, ce XIIIIe mars 1620 » ; 60 Lettre de « THOMAS [FRANÇOIS DE SAVOIE, prince DE CARIGNAN]... à monsieur le duc de Nemours,... A Thurin, ce 19 de mars 1620 » ; 61 Lettre de « V[ITTORE] AMEDEO [prince de Piémont]... à monsieur le duc de Nemours,... A Thurin, ce 19 de mars 1620 » ; 62 Lettre de « V[ITTORE] AMEDEO,... à madame de Nemours,... A Thurin, ce 19 de mars 1620 » ; 63 Lettre du Sr « LE POYVRE » au duc de Nemours. « De Grenoble, le VIe apvril 1620 » ; 64 Lettre de HENRI DE LORRAINE, duc DE « MAYENNE,... à monsieur le duc de Nemours,... De Bourdeaux, ce XVIII apvril 1620 » ; 65 Lettre du Sr DE « GOUMERVILLE,... à monseigneur le duc de Nemours,... De Paris, ce XII juillet 1620 » ; 66 Lettre de « C[LAUDE] FAVRE DE VAUGELAS » au duc de Nemours. « A Paris, ce 14 de septembre 1620 » ; 67 Lettre de « CHRESTIENNE » DE FRANCE, princesse de Piémont, à la duchesse de Nemours. « De Millefleurs, ce 8 octobre » ; 68 Lettre de « RANUCCIO FARNESE [duc DE PARME]... al Sor duca di Nemurs,... Di Parma, 20 ottobre 1620 ». En italien ; 69 « Procuration délivrée par HENRY DE SAVOYE, duc de Genevois, de Nemours et de Chartres », à « Jacques de Montgommery, seigneur de Courbouzon », pour « procedder à l'examen des comptes de Me Claude de Laistre » et « Me Pierre Duclos, intendans » de sa maison, 12 juin 1617. Copie ; 70 Lettre du Sr « CARRON, secretaire de l'ordre » de l'Annonciade, « à monseigneur le duc de Genevois et de Nemors,... De Thurin, ce 20 mars 1621 » ; 71 Lettre d'ALEXANDRE, « cardinale D'ESTE,... al Sor duca di Nemours,... Di Modena, li XXX di marzo 1621 ». En italien ; 72 Lettre du Sr « CARRON, secretaire de l'ordre » de l'Annonciade, « à monseigneur le duc de Genevois et de Nemors,... De Thurin, ce 13 d'avril 1621 » ; 73 Lettre du Sr « CARRON, secretaire de l'ordre » de l'Annonciade, « à monseigneur le duc de Genevois et de Nemors,... De Thurin, ce 10 de juin 1621 » ; 74 Lettre de « GIO[VANNI] RUCHELBRENO » au duc de Nemours. « Di Torino, li 12 di settembre 1621 ». En italien ; 75 Lettre d'«ANNE DE LORRAINE [duchesse DE NEMOURS]... au reverend Pere Comes,... Ce XXVIIIe janvier 1622, à Paris » ; 76 Lettre de « FRANÇOIS DE LORRAINE [comte DE VAUDEMONT]... à monsieur le duc de Nemours,... A Nancy, le XVIme de febvrier 1622 » ; 77 Lettre au duc de Nemours pour l'engager à faire valoir ses droits à la nomination de l'« archevesché d'Auch ». Copie ; 78 Lettre des « president et maistres de la chambre des comptes de Genevoys » à la duchesse de Nemours. « D'Annessy, ce 13 may 1622 » ; 79 Lettre du « prince THOMAS DE SAVOYE » aux « scindicques de la ville d'Annessy », prescrivant « de repartir esgalement les logements des trouppes », avec « ordre d'exemption pour le conseil, la chambre et aultres officiers de monseigneur de Nemours,... A Chambery », 2 juin 1622. Copie ; 80 Lettre de « FRANÇOIS D'ORLEANS [comte DE SAINT-POL]... à monsieur le duc de Nemours,... A Orleans, ce XVe aoust 1622 » ; 81 Lettre de CHARLES DE NEUFVILLE, marquis D'«HALINCOURT,... à monseigneur le duc de Nemours,... De Lion, ce 30e d'aoust 1622 »

Brock Cameo Tie

The Brock cameo tie featuring subtle grey stripes on red was introduced in 1988 in conjunction with the 25th anniversary celebrations of Brock University. The tie is made of polyester from Bradford, England. It originally went on sale for $15.75 in the Bookstore.

Brock University T-shirt

Generic Brock University striped grey shirt.

1970-71 Hockey Team

1970-71 Brock Generals Hockey team. The members from left to right - Back row: Tom Kearney (trainer), Joel Finlay, Tony Grey, Gregg Carrigan, Craig Morrison, Pat Moroney, Rick Charron, Jim Swain, Bill Fuller, Barry Hopkins, Mike McNiven, Rick Sullivan, Ed Barszcz, Phil McCann, Randy Oiling (Manager), Al Kellogg (Coach). Front row: Wayne Butt, Ron Powell, Tim Goodman, Pat McCann, Arkell Farr, Dave Perrin, Gregg Law. Missing: Jeff Della Vedova.

Part of the 1970-71 Hockey Team

Likely a photo of Jim Swain, Tony Grey, Ron Powell, Barry Hopkins, and Joel Finlay circa 1971. (From Left to Right) Second from the right remains unknown.

Structural, stratigraphic and geochemical studies of the Horwood Peninsula - Gander Bay Area, Northeast Newfoundland /

The Horwood Peninsula - Gander Bay area is located at NE Newfoundland in the Botwood Zone (Williams et a1., 1974) or in the Dunnage Zone (Williams, 1979) of the Central Mobile Belt of the Newfoundland Appalachians. The area is underlain by Middle Ordovician to possible Lower Silurian rocks of the Davidsville and Indian Islands Groups, respectively. Three conformable formations named informally : the Mafic Volcanic Formation, the Greywacke and Siltstone Formation and the Black Slate Formation, have been recognized in the Davidsville Group. The Greywacke and the Black Slate Formations pass locally into a Melange Formation. From consideration of regional structure and abundant locally-derived mafic volcanic olisto- 1iths in the melange, it is considered to have originated by gravity sliding rather than thrusting. Four formations have been recognized in the Indian Islands Group. They mainly contain silty slate and phyllite, grey cherty siltstone, green to red micaceous siltstone and limestone horizons. Repetition of lithological units by F1 folding are well-demonstrated in one of formations in this Group. The major structure in this Group on the Horwood Peninsula is interpreted to be a synclinal complex. The lithology of this Group is different from the Botwood Group to the west and is probably Late Ordovician and/or Early Silurian in age. The effects of soft-sediment deformation can be seen from the lower part of the Davidsville Group to the middle part of the Indian Islands Group indicating continuous and/or episodic slumping and sliding activities throughout the whole area. However, no siginificant depOSitional and tectonic break that could be assigned to the Taconian Orogeny has been recognized in this study. Three periods of tectonic deformation were produced by the Acadian Orogeny. Double boudinage in thin dikes indicates a southeast-northwest sub-horizontal compression and main northeast-southwest sub-horizontal extension during the D1 deformation. A penetrative, axial planar slaty cleavage (Sl) and tight to isocJ.ina1 F1 folds are products of this deformation. The D2 and D3 deformations formed S2 and S3 fabrics associated with crenulations and kink bands which are well-shown in the slates and phyllites of the Indian Islands Group. The D2 and D3 deformations are the products of vertical and northeast-southwest horizontal shortening respectively. The inferred fault between the Ordovician slates (Davidsville Group) and the siltstones (Indian Islands Group) suggested by Williams (1963, 1964b, 1972, 1978) is absent. Formations can be followed without displacement across this inferred fault. Chemically, the pillow lavas, mafic agglomerates, tuff beds and diabase dikes are subdivided into three rock suites : (a) basaltic komatiite (Beaver Cove Assemblage), (b) tholeiitic basalt (diabase dikes), (c) alkaline basalt (Shoal Bay Assemblage). The high Ti02 , MgO, Ni contents and bimodal characteristic of the basaltic komatiite in the area are comparable to the Svartenhuk Peninsula at Baffin Bay and are interpreted to be the result of an abortive volcano-tectonic rift-zone in a rear-arc basin. Modal and chemical analyses of greywackes and siltstones show the trend of maturity of these rocks increasing from poorly sorted Ordovician greywackes to fairly well-sorted Silurian siltstones. Rock fragments in greywackes indicate source areas consisting of plagiogranite, low grade metamorphic rocks and ultramafic rocks. Rare sedimentary structures in both Groups indicate a southeasterly provenance. Trace element analyses of greywackes also reveal a possible island-arc affinity.

The effects of static and diurnally-cycling temperature acclimations on thermal tolerances of rainbow trout, Salmo gairdneri

:ofiedian lethal temperatures ( LT50' s ) were determined for rainbow trout, Salmo gairdnerii, acclimated for a minimum of 21 days at 5 c onstant temperatures between 4 and 20 0 C. and 2 diel temperature fluctuations ( sinewave curves of amplitudes ± 4 and ± 7 0 C. about a mean temperature of 12 0 C. ) . Twenty-four-, 48-, and 96-hour LT50 estimates were c alculated f ollowing standard flow-through aquatic bioassay techniques and probi t transformation of mortality data. The phenomenon of delayed thermal mortality was also investigated. Shifts in upper incipient lethal temperature occurred as a result of previous thermal conditioning. It was shown that increases in constant acclimation temperature result in proportional l inear increases in thermal tolerances. The increase i n estimated 96-hour LT50's was approximately 0.13 0 c. X 1 0 C:1 between 8 and 20 0 C. The effect of acclimation to both cyclic temperature regimes was an increase in LT50 to values between the mean and maximum constant equivalent daily temperatures of the cycles. Twenty-four-, 48-, and 96-hour LT50 estimates of both cycles corresponded approximately to the LT50 values of the 16 0 C. c onstant temperature equivalent . This increase i n thermal tolerance was further demonstrated by the delayed thermal mortality experiments . Cycle amplitudes appeared to i nfluence thermal resistance through alterations in initi al mortality since mortality patterns characteristic of base temperature acclimations re-appeared after approximately 68 hours exposure to test temperatures for the 12 + 4 0 C. group, whereas mortality patterns stabilized and remained constant for a period greater than 192 hours with the larger therma l cycle ( 12 + 7 0 C. ). NO s ignificant corre lations between s pecimen weight and time-to-death was apparent. Data are discussed in relation to the establishment of thermal criteria for important commercial and sport fishes , such as the salmonids , as is the question whether previously reported values on lethal temperature s may have been under estimated.